Abstract
Benzoxazinoids (BXs), such as 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA), are secondary metabolites in grasses. The first step in BX biosynthesis converts indole-3-glycerol phosphate into indole. In maize (Zea mays), this reaction is catalyzed by either BENZOXAZINELESS1 (BX1) or INDOLE GLYCEROL PHOSPHATE LYASE (IGL). The Bx1 gene is under developmental control and is mainly responsible for BX production, whereas the Igl gene is inducible by stress signals, such as wounding, herbivory, or jasmonates. To determine the role of BXs in defense against aphids and fungi, we compared basal resistance between Bx1 wild-type and bx1 mutant lines in the igl mutant background, thereby preventing BX production from IGL. Compared to Bx1 wild-type plants, BX-deficient bx1 mutant plants allowed better development of the cereal aphid Rhopalosiphum padi, and were affected in penetration resistance against the fungus Setosphaeria turtica. At stages preceding major tissue disruption, R. padi and S. turtica elicited increased accumulation of DIMBOA-glucoside, DIMBOA, and 2-hydroxy-4,7-dimethoxy-1,4-benzoxazin-3-one-glucoside (HDMBOA-glc), which was most pronounced in apoplastic leaf extracts. Treatment with the defense elicitor chitosan similarly enhanced apoplastic accumulation of DIMBOA and HDMBOA-glc, but repressed transcription of genes controlling BX biosynthesis downstream of BX1. This repression was also obtained after treatment with the BX precursor indole and DIMBOA, but not with HDMBOA-glc. Furthermore, BX-deficient bx1 mutant lines deposited less chitosan-induced callose than Bx1 wild-type lines, whereas apoplast infiltration with DIMBOA, but not HDMBOA-glc, mimicked chitosan-induced callose. Hence, DIMBOA functions as a defense regulatory signal in maize innate immunity, which acts in addition to its well-characterized activity as a biocidal defense metabolite.
Highlights
Benzoxazinoids (BXs), such as 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA), are secondary metabolites in grasses
DIBOA-glc and DIMBOA-glc can be hydrolyzed by two plastid-targeted b-glucosidases, ZmGLU1 and ZmGLU2 (Cicek and Esen, 1999; Czjzek et al, 2001), which causes the release of biocidal DIBOA and DIMBOA aglycones
The bx1 single mutant is unsuitable to assess the contribution of BXs to resistance against jasmonic acid (JA)-eliciting attackers, such as R. padi and S. turtica (Delp et al, 2009; Erb et al, 2009)
Summary
Benzoxazinoids (BXs), such as 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA), are secondary metabolites in grasses. It is commonly assumed that BX-glucosides are hydrolyzed by plastid-targeted b-glucosidases upon tissue disruption, which results in the release of biocidal aglycone BXs (Morant et al, 2008) Since their discovery as plant secondary metabolites, many investigations have focused on their role in plant defense against herbivorous insects and pathogens (Niemeyer, 1988, 2009). DIBOA-glc and DIMBOA-glc can be hydrolyzed by two plastid-targeted b-glucosidases, ZmGLU1 and ZmGLU2 (Cicek and Esen, 1999; Czjzek et al, 2001), which causes the release of biocidal DIBOA and DIMBOA aglycones This mode of action is consistent with a role for BXs in resistance against chewing herbivores that cause major tissue damage. BXs have been implicated in defense against aphids and pathogenic fungi that cause relatively little tissue damage (Niemeyer, 2009), which suggests an alternative mechanism of BX-dependent resistance
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